1. The purpose of the present study was to examine the effect of a plantarflexor maximum voluntary contraction (MVC) on Achilles tendon moment arm length.
2. Sagittal magnetic resonance (MR) images of the right ankle were taken in six subjects both at rest and during a plantarflexor MVC in the supine position at a knee angle of 90 deg and at ankle angles of -30 deg (dorsiflexed direction), -15 deg, 0 deg (neutral ankle position), +15 deg (plantarflexed direction), +30 deg and +45 deg. A system of mechanical stops, support triangles and velcro straps was used to secure the subject in the above positions. Location of a moving centre of rotation was calculated for ankle rotations from -30 to 0 deg, -15 to +15 deg, 0 to +30 deg and +15 to +45 deg. All instant centres of rotation were calculated both at rest and during MVC. Achilles tendon moment arms were measured at ankle angles of -15, 0, +15 and +30 deg.
3. At any given ankle angle, Achilles tendon moment arm length during MVC increased by 1-1.5 cm (22-27 %, P < 0.01) compared with rest. This was attributed to a displacement of both Achilles tendon by 0.6-1.1 cm (P < 0.01) and all instant centres of rotation by about 0.3 cm (P < 0.05) away from their corresponding resting positions.
4. The findings of this study have important implications for estimating loads in the musculoskeletal system. Substantially unrealistic Achilles tendon forces and moments generated around the ankle joint during a plantarflexor MVC would be calculated using resting Achilles tendon moment arm measurements.
In this research published in Journal of Physiology Anthony Sargeant and his team describe how the recruitment of different types of muscle fibres with increasing exercise intensity changes the oxygen cost of exercise. Thus the relationship of oxygen uptake and mechanical power output is not constant. This is in contrast to the standard teaching of many physiology textbooks.
1. A slow component to pulmonary oxygen uptake (VO2) is reported during prolonged high power exercise performed at constant power output at, or above, approximately 60% of the maximal oxygen uptake. The magnitude of the slow component is reported to be associated with the intensity of exercise and to be largely accounted for by an increased VO2 across the exercising legs.
2. On the assumption that the control mechanism responsible for the increased VO2 is intensity dependent we hypothesized that it should also be apparent in multi-stage incremental exercise tests with the result that the VO2-power output relationship would be curvilinear.
3. We further hypothesized that the change in the VO2-power output relationship could be related to the hierarchical recruitment of different muscle fibre types with a lower mechanical efficiency.
4. Six subjects each performed five incremental exercise tests, at pedalling rates of 40, 60, 80, 100 and 120 rev min-1, over which range we expected to vary the proportional contribution of different fibre types to the power output. Pulmonary VO2 was determined continuously and arterialized capillary blood was sampled and analysed for blood lactate concentration ([lactate]b).
5. Below the level at which a sustained increase in [lactate]b was observed pulmonary VO2 showed a linear relationship with power output; at high power outputs, however, there was an additional increase in VO2 above that expected from the extrapolation of that linear relationship, leading to a positive curvilinear VO2-power output relationship. 6. No systematic effect on the magnitude or onset of the ‘extra’ VO2 was found in relation to pedalling rate, which suggests that it is not related to the pattern of motor unit recruitment in any simple way.
Cycling performance depends upon overcoming air and rolling resistance in this research the results of ‘coasting down’ experiments were used by the authors to calculate these components. The experiments were performed in the massive indoor Flower Hall near Amsterdam on a Sunday morning. Anthony Sargeant was the head of the research department which carried out this work.
To calculate the power output during actual cycling, the air friction force Fa and rolling resistance Fr have to be known. Instead of wind tunnel experiments or towing experiments at steady speed, in this study these friction forces were measured by coasting down experiments. Towing experiments at constant acceleration (increasing velocity) were also done for comparison. From the equation of motion, the velocity-time curve v(t) was obtained. Curve-fitting procedures on experimental data of the velocity v yielded values of the rolling resistance force Fr and of the air friction coefficient k = Fa/v2. For the coasting down experiments, the group mean values per body mass m (N = 7) were km = k/m = (2.15 +/- 0.32) x 10(-3)m-1 and ar = Fr/m = (3.76 +/- 0.18) x 10(-2)ms-2, close to other values from the literature. The curves in the phase plane (velocity vs acceleration) and the small residual sum of squares indicated the validity of the theory. The towing experiments were not congruent with the coasting down experiments. Higher values of the air friction were found, probably due to turbulence of the air.
Anita Beelen presented this research as part of her PhD thesis supervised by Professor Anthony Sargeant. Uniquely the study used electrical stimulation superimposed upon on maximal voluntary activation in dynamic exercise.
1. Percutaneous electrical stimulation of the human quadriceps muscle has been used to assess the loss of central activation immediately after a bout of fatiguing exercise and during the recovery period.
2. Fatigue was induced in eight healthy males by a maximal effort lasting 25 s performed on an isokinetic cycle ergometer at a constant pedal frequency of 60 revolutions per minute. The cranks of the ergometer were driven by an electric motor. Before and after the sprint, subjects allowed their legs to be passively taken round by the motor. During the passive movement the knee extensors were stimulated (4 pulses; 100 Hz). Peak voluntary force (PVF) during the sprint and peak stimulated forces (PSF) before and in recovery were recorded via strain gauges in the pedals. Recovery of voluntary force was assessed in a series of separate experiments in which subjects performed a second maximal effort after recovery periods of different durations.
3. Peak stimulated forces were reduced to 69f8 + 9 3 % immediately after the maximal effort, (P< 0 05), but had returned to pre-exercise values after 3 min. The maximum rate of force development (MRFD) was also reduced following fatigue to 68f8 + 11 0% (P < 0’05) of control and was fully recovered after 2 min. PVF was reduced to 72-0 + 9 4% (P< 0 05) of the control value following the maximal effort. After 3 min voluntary force had fully recovered.
4. The effect of changing the duration of the fatiguing exercise (10, 25 and 45 s maximal effort) resulted in an increased degree of voluntary force loss as the duration of the maximal effort increased. This was associated with an increased reduction in PSF measured immediately after the exercise.
5. The close association between the changes in stimulated force and voluntary force suggests that the fatigue in this type of dynamic exercise may be due to changes in the muscle itself and not to failure of central drive.
In this important series of studies a collaboration between the research group in Amsterdam led by Anthony Sargeant and that in London under the direction of Professor Geoffrey Goldspink used new techniques based on microdissection of fragments of human muscle fibre obtained by needle biopsy.
Using a method of single muscle fibre analysis, we investigated the presence of RNA transcripts for various isoforms of the myosin heavy chain (MyoHC) gene in histochemically, immunohistochemically and electrophoretically characterized individual muscle fibres (n = 65) from adult human vastus lateralis muscle. A cDNA clone isolated in this study was shown to contain the 3′ end of a previously uncharacterized human MyoHC gene which is expressed specifically in human fast IIA muscle fibres and we conclude that this clone contains part of the human fast IIA MyoHC gene. In all the fibres histochemically, immunohistochemically and electrophoretically characterized as containing the previously classified IIB MyoHC (n = 23), it was shown that the human equivalent to the rat type IIX MyoHC gene is expressed. This observation was taken to suggest that the previously classified IIB muscles fibres in human muscle express a MyoHC isoform equivalent to the rat IIX, not the IIB, and would therefore be more accurately classified as IIX fibres.
This research publication describes a method developed in the Amsterdam Department of Anthony Sargeant. The data was collected by an outstanding Greek PhD student, Christina Karatzaferi, directed by Tony and his colleague Arnold de Haan.
Abstract A sensitive and reproducible method for the determination of adenine nucleotides (ATP, IMP) and creatine compounds [creatine (Cr), phosphocreatine (PCr)] in freeze-dried single human muscle fibre fragments is presented. The method uses isocratic reversed-phase high-performance liquid chromatography of methanol extracts. Average retention times (min) of ATP, IMP and PCr, Cr from standard solutions were 10.6+/-0.42, 2.11+/-0.06 (n=6) and 10.5+/-0.31 and 1.19+/-0.02 (n=9), respectively. Detection limits in extracts from muscle fibre fragments were 2.0, 1.0, 3.0 and 2.0 mmol/kg dm, respectively. The assay was found successful for analysis of fibre-fragments weighing > or = 1 microg.
As head of department Anthony Sargeant had spent many years encouraging his junior colleagues to adapt a technique used to measure muscle force in a rat muscle preparation to measure electrically elicited force in human hand muscles. Finally collaborating with Professor David A Jones (a friend and colleague with a lot of experience in electrical stimulation of human muscle) Tony finally got colleagues to develop the technique reported in this research paper. David Jones and Anthony Sargeant both acted as subjects and provided critical input in the experiments for the development and application of these techniques.
The purpose of the study was to obtain force/velocity relationships for electrically stimulated (80 Hz) human adductor pollicis muscle (n = 6) and to quantify the effects of fatigue. There are two major problems of studying human muscle in situ; the first is the contribution of the series elastic component, and the second is a loss of force consequent upon the extent of loaded shortening. These problems were tackled in two ways.
Records obtained from isokinetic releases from maximal isometric tetani showed a late linear phase of force decline, and this was extrapolated back to the time of release to obtain measures of instantaneous force. This method gave usable data up to velocities of shortening equivalent to approximately one-third of maximal velocity. An alternative procedure (short activation, SA) allowed the muscle to begin shortening when isometric force reached a value that could be sustained during shortening (essentially an isotonic protocol). At low velocities both protocols gave very similar data (r2 = 0.96), but for high velocities only the SA procedure could be used. Results obtained using the SA protocol in fresh muscle were compared to those for muscle that had been fatigued by 25 s of ischaemic isometric contractions, induced by electrical stimulation at the ulnar nerve. Fatigue resulted in a decrease of isometric force [to 69 (3)%], an increase in half-relaxation time [to 431 (10)%], and decreases in maximal shortening velocity [to 77 (8)%] and power [to 42 (5)%]. These are the first data for human skeletal muscle to show convincingly that during acute fatigue, power is reduced as a consequence of both the loss of force and slowing of the contractile speed.